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KMID : 0624620200530110582
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BMB Reports
2020 Volume.53 No. 11 p.582 ~ p.587
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Tat-indoleamine 2,3-dioxygenase 1 elicits neuroprotective effects on ischemic injury
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Park Jung-Hwan
Kim Dae-Won
Shin Min-Jea
Park Jin-Seu
Han Kyu-Hyung
Lee Keun-Wook
Park Jong-Kook
Choi Yeon-Joo
Yeo Hyeon-Ji
Yeo Eun-Ji
Sohn Eun-Jeong
Kim Hyoung-Chun
Shin Eun-Joo
Cho Sung-Woo
Kim Duk-Soo
Cho Yong-Jun
Eum Won-Sik
Choi Soo-Young
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Abstract
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It is well known that oxidative stress participates in neuronal cell death caused production of reactive oxygen species (ROS). The increased ROS is a major contributor to the development of ischemic injury. Indoleamine 2,3-dioxygenase 1 (IDO-1) is involved in the kynurenine pathway in tryptophan metabolism and plays a role as an anti-oxidant. However, whether IDO-1 would inhibit hippocampal cell death is poorly known. Therefore, we explored the effects of cell permeable Tat-IDO-1 protein against oxidative stress-induced HT-22 cells and in a cerebral ischemia/reperfusion injury model. Transduced Tat-IDO-1 reduced cell death, ROS production, and DNA fragmentation and inhibited mitogen-activated protein kinases (MAPKs) activation in H2O2 exposed HT-22 cells. In the cerebral ischemia/ reperfusion injury model, Tat-IDO-1 transduced into the brain and passing by means of the blood-brain barrier (BBB) significantly prevented hippocampal neuronal cell death. These results suggest that Tat-IDO-1 may present an alternative strategy to improve from the ischemic injury.
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KEYWORD
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Ischemia, MAPKs, Oxidative stress, Protein therapy, Tat-IDO-1
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